Cargando…

A high level of lncFGD5-AS1 inhibits epithelial-to-Mesenchymal transition by regulating the miR-196a-5p/SMAD6/BMP axis in gastric Cancer

BACKGROUND: Long non-coding RNA (lncRNA) was a vital factor in the progression and initiation of human cancers. This study found a new lncRNA, FGD5-AS1, which can inhibit EMT process, proliferation, and metastasis in vitro and in vivo. METHODS: qRT-PCR was employed to test the expression of lncFGD5-...

Descripción completa

Detalles Bibliográficos
Autores principales: Liu, Lin, Zhang, Cheng, Wang, Jizhao, Liu, Xu, Qu, Hangying, Zhang, Guangjian, Liang, Ting, Wang, Jiansheng, Zhang, Jia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8066889/
https://www.ncbi.nlm.nih.gov/pubmed/33892661
http://dx.doi.org/10.1186/s12885-021-08192-x
_version_ 1783682673338744832
author Liu, Lin
Zhang, Cheng
Wang, Jizhao
Liu, Xu
Qu, Hangying
Zhang, Guangjian
Liang, Ting
Wang, Jiansheng
Zhang, Jia
author_facet Liu, Lin
Zhang, Cheng
Wang, Jizhao
Liu, Xu
Qu, Hangying
Zhang, Guangjian
Liang, Ting
Wang, Jiansheng
Zhang, Jia
author_sort Liu, Lin
collection PubMed
description BACKGROUND: Long non-coding RNA (lncRNA) was a vital factor in the progression and initiation of human cancers. This study found a new lncRNA, FGD5-AS1, which can inhibit EMT process, proliferation, and metastasis in vitro and in vivo. METHODS: qRT-PCR was employed to test the expression of lncFGD5-AS1 in 30 gastric cancer patients’ cancer tissue and para-cancer tissue. Overexpressed lncFGD5-AS1 cells shown sharply decrease of proliferation, migration, and epithelial-mesenchymal transition (EMT). miR-196a-5p/SMAD6 was confirmed as downstream molecular mechanism of lncFGD5-AS1 by expression correlation analysis and mechanism experiments. In vivo study illustrated overexpression of lncFGD5-AS1 suppression tumor growth. RESULTS: LncFGD5-AS1 served as a ceRNA of miR-196a-5p to release its inhibition on SMAD6, a conventional inhibitor on the BMP pathway. Comparing with normal gastric cancer cells, FGD5-AS1 overexpressed group had fewer migration cells, lower cell viability, and lower EMT transformation rate. Meanwhile, xenografts nude mice injecting with overexpressed-FGD5-AS1 cells also shown smaller tumor weight and volume. CONCLUSION: In conclusion, this research supported the first evidence that FGD5-AS1 suppressed proliferation and metastasis in gastric cancer by regulating miR-196a-5p/SMAD6/BMP axis and suggested a potential therapeutic candidate for gastric cancer. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-021-08192-x.
format Online
Article
Text
id pubmed-8066889
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-80668892021-04-26 A high level of lncFGD5-AS1 inhibits epithelial-to-Mesenchymal transition by regulating the miR-196a-5p/SMAD6/BMP axis in gastric Cancer Liu, Lin Zhang, Cheng Wang, Jizhao Liu, Xu Qu, Hangying Zhang, Guangjian Liang, Ting Wang, Jiansheng Zhang, Jia BMC Cancer Research Article BACKGROUND: Long non-coding RNA (lncRNA) was a vital factor in the progression and initiation of human cancers. This study found a new lncRNA, FGD5-AS1, which can inhibit EMT process, proliferation, and metastasis in vitro and in vivo. METHODS: qRT-PCR was employed to test the expression of lncFGD5-AS1 in 30 gastric cancer patients’ cancer tissue and para-cancer tissue. Overexpressed lncFGD5-AS1 cells shown sharply decrease of proliferation, migration, and epithelial-mesenchymal transition (EMT). miR-196a-5p/SMAD6 was confirmed as downstream molecular mechanism of lncFGD5-AS1 by expression correlation analysis and mechanism experiments. In vivo study illustrated overexpression of lncFGD5-AS1 suppression tumor growth. RESULTS: LncFGD5-AS1 served as a ceRNA of miR-196a-5p to release its inhibition on SMAD6, a conventional inhibitor on the BMP pathway. Comparing with normal gastric cancer cells, FGD5-AS1 overexpressed group had fewer migration cells, lower cell viability, and lower EMT transformation rate. Meanwhile, xenografts nude mice injecting with overexpressed-FGD5-AS1 cells also shown smaller tumor weight and volume. CONCLUSION: In conclusion, this research supported the first evidence that FGD5-AS1 suppressed proliferation and metastasis in gastric cancer by regulating miR-196a-5p/SMAD6/BMP axis and suggested a potential therapeutic candidate for gastric cancer. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-021-08192-x. BioMed Central 2021-04-23 /pmc/articles/PMC8066889/ /pubmed/33892661 http://dx.doi.org/10.1186/s12885-021-08192-x Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Liu, Lin
Zhang, Cheng
Wang, Jizhao
Liu, Xu
Qu, Hangying
Zhang, Guangjian
Liang, Ting
Wang, Jiansheng
Zhang, Jia
A high level of lncFGD5-AS1 inhibits epithelial-to-Mesenchymal transition by regulating the miR-196a-5p/SMAD6/BMP axis in gastric Cancer
title A high level of lncFGD5-AS1 inhibits epithelial-to-Mesenchymal transition by regulating the miR-196a-5p/SMAD6/BMP axis in gastric Cancer
title_full A high level of lncFGD5-AS1 inhibits epithelial-to-Mesenchymal transition by regulating the miR-196a-5p/SMAD6/BMP axis in gastric Cancer
title_fullStr A high level of lncFGD5-AS1 inhibits epithelial-to-Mesenchymal transition by regulating the miR-196a-5p/SMAD6/BMP axis in gastric Cancer
title_full_unstemmed A high level of lncFGD5-AS1 inhibits epithelial-to-Mesenchymal transition by regulating the miR-196a-5p/SMAD6/BMP axis in gastric Cancer
title_short A high level of lncFGD5-AS1 inhibits epithelial-to-Mesenchymal transition by regulating the miR-196a-5p/SMAD6/BMP axis in gastric Cancer
title_sort high level of lncfgd5-as1 inhibits epithelial-to-mesenchymal transition by regulating the mir-196a-5p/smad6/bmp axis in gastric cancer
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8066889/
https://www.ncbi.nlm.nih.gov/pubmed/33892661
http://dx.doi.org/10.1186/s12885-021-08192-x
work_keys_str_mv AT liulin ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT zhangcheng ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT wangjizhao ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT liuxu ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT quhangying ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT zhangguangjian ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT liangting ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT wangjiansheng ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT zhangjia ahighleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT liulin highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT zhangcheng highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT wangjizhao highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT liuxu highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT quhangying highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT zhangguangjian highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT liangting highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT wangjiansheng highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer
AT zhangjia highleveloflncfgd5as1inhibitsepithelialtomesenchymaltransitionbyregulatingthemir196a5psmad6bmpaxisingastriccancer